The major goal of this project is to examine the mechanisms of salt appetite under conditions in which sodium deficiency is not the precipitating factor. It is the specific hypothesis of this project that renal escape and the increased salt appetite that follow mineralcorticoid administration are related phenomena and due to the same natriuretic mechanism. In the proposed experiments we will use radioimmunoassay (RIA) procedures, acute and chronic infusions and electrophysiological recordings to determine the relationship between endogenous natriuretic agents and the changes in sodium balance and intake that occur after the administration of DOCA, ACTH or high salt diet to sodium replete rats and hamsters, and that occur normally in spontaneously hypertensive (SHR) rats. Highest priority will be given to the study of atrial natriuretic factor (ANF), but the possible role of gamma-melanocyte stimulating hormone (gamma-MSH) and vanadate (Na3VO4) will also be considered as developments warrant. The proposed studies are designed to answer the following question: 1) Are plasma levels of ANF increased with the changes in sodium balance and intake that occur after the administration of DOCA or ACTH? 2) Is renal escape and increased salt intake in response to DOCA or ACTH suppressed in normal rats by reducing plasma levels of ANF by immunoneutralization, alone or in conjunction with surgical removal of the atrial appendates? 3) Are plasma levels of ANF decrased in a strain of myopathic (BIO 14.6) hamsters whose atria are deficient in ANF activity and who do not show signs of renal escape or develop salt appetite in response to DOCA administration? 4) Can renal escape and salt appetite be made to develop in the same hamsters by chronically infusing synthetic ANF along with DOCA administration? 5) Does chronic infusion of ANF, gamma-MSH or vanadate increase salt intake in sodium replete rats and are the effects specific to sodium? 6) Are neural taste responses reduced in the four chosen models of salt appetite; are these changes specific to sodium and do they occur when the animals are not given access to salt solutions? 7) Does acute infusion of ANF, gamma-MSH or vanadate reduce taste neural responses in a manner that parallels the decreased renal sodium reabsorption produced by these agents, and are these changes specific to sodium?